Congestive heart failure (CHF) is a common heart disease, which is recognized as the most common cause of hospitalization and mortality in Western society. CHF is an extremely serious affliction that has a great impact on the quality of life. CHF develops generally in the course of months or years, and can be the end stage of chronic hypertension, infarction, angina, or diabetes. The prevalence of incidents of congestive heart failure has recently increased, and there is considerable morbidity and mortality-associated with its diagnosis. In fact, congestive heart failure is an extremely lethal disease with an estimated five-year mortality for a vast majority of both men and women who encounter the disease.
Congestive heart failure refers to a situation in which the ventricle pumps less blood than a healthy ventricle under the same conditions. The rate at which blood is delivered to the left or right atrium thus exceeds the rate at which blood is pumped out of the heart by the left or right ventricle, respectively.
Congestive heart failure is primarily characterized by ventricular dysfunction. The decreased contractility of the left ventricle leads to reduced cardiac output with consequent systemic arterial and venous vasoconstriction. Ventricular diastolic dysfunction is the inability of the ventricle walls to expand and to fill the ventricle with the same blood volume as a healthy ventricle under the same conditions. Ventricular systolic dysfunction is the inability of the ventricle to contract and push the same blood volume as a healthy ventricle under the same conditions.
Another cause of congestive heart failure is mitral valve dysfunction. The cause of mitral valve dysfunction are mitral insufficiency, mitral stenosis or a combination of these. Mitral insufficiency means that the valve does not completely close. Mitral stenosis means that the valve does not open enough to enable the desired blood flow into the left ventricle.
One consequence of CHF is pulmonary edema, in which fluid accumulates in the lungs due to a higher blood flow rate in the pulmonary arteries than in the pulmonary veins. As pressure in the pulmonary veins rises, fluid is pushed into the air spaces (alveoli). This fluid then becomes a barrier to normal gas exchange in the alveoli, resulting in shortness of breath. This sequence of events results in hypoxemia, hypercapnia, and death.
Dyspnea in patients with CHF appears often at night when the patient is lying and the venous return is increased. This nocturnal dyspnea endangers the patient. Usually is alleviated when the patient sits or stands up.
Presently available treatments for CHF fall into three generally categories: (1) pharmacological, e.g., diuretics; (2) assist systems, e.g., pumps; (3) surgical treatments; and (4) resynchronization.
With respect to pharmacological treatments, diuretics have been used to reduce the workload of the heart by reducing blood volume. While drug treatment improves quality of life, it has little effect on survival. Current pharmacological treatment includes a combination of diuretics, vasodilators, inotropes, beta-blockers, and Angiotensin Converting Enzyme (ACE) inhibitors. The effect is a decrease of symptoms, and improved quality of life, but little change in mortality.
Cardiac assist devices used to treat CHF include, for example, mechanical pumps. Mechanical pumps reduce the load on the heart by performing all or part of the pumping function normally done by the heart. Currently, mechanical pumps are used to sustain the patient until a donor heart for transplantation becomes available for the patient. There are also a number of pacing devices used to treat CHF.
There are at least three surgical procedures for treatment of heart failure: 1) heart transplant; 2) dynamic cardiomyoplasty; and 3) left ventriculectomy. Heart transplantation has serious limitations including restricted availability of organs and the adverse effects of immunosuppressive therapies required following heart transplantation. Cardiomyoplasty includes wrapping the heart with skeletal muscle and electrically stimulating the muscle to contract synchronously with the heart in order to help the pumping function of the heart. Left ventriculectomy includes surgically remodeling the left ventricle by removing a segment of the muscular wall. This procedure reduces the diameter of the dilated heart, which in turn reduces the loading of the heart. However, this extremely invasive procedure reduces muscle mass of the heart.
Finally, cardiac resynchronization therapy can be delivered by a cardiac rhythm management device in accordance with a bradycardia pacing mode so that the selected heart chambers are both resynchronized and paced simultaneously.
U.S. Published Patent Application No. 2002/0173742 to Keren et al. describes a shunt for decreasing pressure in a portion of the left ventricle of a patient. The shunt is implanted whereby a volume of blood is released that is sufficient to reduce end diastolic pressure in the left ventricle.
U.S. Pat. No. 5,509,888 to Miller describes a device for regulating fluid flow within a body tube such as a blood vessel. The device includes a ring that is positioned around the body tube. The caliber of the ring is under the control of a programmable control unit. Decreasing the caliber of the ring constricts the body tube thus decreasing the flow of fluid in the body tube.
WO 01/72239 describes an implant adapted for insertion into blood vessels for reducing the diameter of a blood vessel. The implant is used, for example, in a coronary sinus or other coronary vein to reduce the flow rate of blood in the vessel.
U.S. Pat. Nos. 6,280,377 and 6,086,527 to Talpade describe a system for regulating blood flow to a portion of the vasculature, such as the renal system, in order to treat heart disease. Blood flow in the portion of the vasculature is regulated so as to control physiological feedback responses to high or low blood pressure, in order to relieve overload conditions on the heart. Increasing blood flow to the renal arteries thus inhibiting the renal response to hypotension and inhibiting the vascorestriction and increased blood volume associated with that response. This reduces the overload and stress on the heart, thus allowing passive rehabilitation of the myocardial system.
U.S. Pat. No. 6,473,647 to Bradley describes an implantable cardiac stimulation device that monitors progression or regression in a patient's heart disease. A pulse generator delivers pacing pulses to the heart to cause responses of the heart. A sensing circuit senses the responses of the heart and generates response signals. A processor is programmed to analyze the response signals, to isolate a given characteristic of the response signals and to quantify the isolated characteristics to provide corresponding quantized values. Relative changes in the quantized values over time are indicative of the progression or regression in the patient's heart disease. A memory stores the quantized values and a telemetry circuit transmits the stored quantized values to an external receiver for analysis.
U.S. Pat. No. 6,507,756 to Heynen et al describes rate responsive pacing systems that employ a time-dependent atrial-ventricular (AV) delay. A starting or initial AV delay is set to an intrinsic AV delay time interval exhibited by the patient's heart at the time of implant. A chronic AV delay is then set to a therapeutic AV delay time interval that is shorter than the intrinsic AV delay time interval. A Time-Adaptive AV delay (TA-AV delay) is employed during a post-implant Time-Adaptive period that gradually changes the initial AV delay to the chronic AV delay at the end of the post-implant Time-Adaptive period.
U.S. Pat. No. 6,275,727 to Hopper et al describes a method and apparatus for providing congestive heart failure therapy status. An electronic device, preferably a cardiac rhythm management device, capable of measuring transthoracic impedance and for sensing a level of physical activity is implanted in a patient. The transthoracic impedance signal is processed to obtain an estimate of the subject's minute ventilation, respiratory rate and tidal volume. From accelerometer measured activity, an estimate is obtained of oxygen uptake and carbon dioxide production. Ratios of tidal volume to respiratory rate, tidal volume to inspiratory time, minute ventilation to carbon dioxide production and oxygen uptake to heart rate are meaningful status indicators for assessing the efficacy of particular therapy regimens to CHF patients.
U.S. Pat. No. 6,422,990 to Prem describes a method and apparatus for use with a blood pump. Multiple sensors are positioned around the ventricle. Based on the measurements of the sensors it is possible to calculate either a cross sectional area or a volume of the ventricle during distension and contraction. The calculated area or volume is indicative of distension and contraction than a single radial dimension measurement. The area or volume can be utilized to control the blood pump flow rate to avoid overly distending or contracting the ventricle and for operating the flow rate in a pulsatile manner to closely approximate the natural pumping action of the heart.